Specific changes in hepatic gene expression following resuscitation from cardiogenic shock are identified. Aberrantly sustained or prematurely terminated programs of liver gene expression account for the dysregulated metabolism of multiple organ system failure. Having shown that cardiogenic shock induces several transcriptional programs which are mutually exclusive and which have an intrinsic hierarchy, he proposes to identify which hepatic transcriptional programs are regulated during the hypermetabolic state of late MOSF and to define the molecular mechanisms responsible for their persistence or termination. Comparing heart tamponade and E. coli IP swine shock models, he will: (1) Show whether the differences noted in the hepatic transcriptional programs 8 hours after cardiogenic shock versus late sepsis are due to the types of shock, "ebb" versus "flow" or both; (2) Find the mechanism for the transcriptional shutoff of the genes apparently specific for cardiogenic shock and (3) Identify those genes transcribed during hypermetabolic late sepsis which are not transcribed during early cardiogenic shock and then define their regulatory mechanisms.